Beihua Zhong1, Shuangtao Ma1, Donna H Wang2,3,4. 1. Division of Nanomedicine and Molecular Intervention, Department of Medicine, Michigan State University, East Lansing, MI, U.S.A. 2. Division of Nanomedicine and Molecular Intervention, Department of Medicine, Michigan State University, East Lansing, MI, U.S.A. wangdo@msu.edu. 3. Neuroscience Program, Michigan State University, East Lansing, MI, U.S.A. 4. Cell & Molecular Biology Program, Michigan State University, East Lansing, MI, U.S.A.
Abstract
BACKGROUND/AIM: Transient receptor potential vanilloid type 1 (TRPV1) has anti-inflammatory properties. The present study aimed to investigate the role of TRPV1 in renal inflammatory responses and tissue injury following renal ischemia-reperfusion (I/R) in diet-induced obese mice. MATERIALS AND METHODS: TRPV1 knockout and wild type mice were fed a normal or western diet (WD) for 23 weeks and were then subjected to renal I/R injury. RESULTS: TRPV1 knockout mice showed enhanced WD-induced renal macrophage infiltration and collagen deposition. Knocking out TRPV1 exacerbated renal I/R-induced increase of malondialdehyde, interleukin-6, monocyte chemoattractant protein-1, and NF-ĸB in obese mice. Similar results were observed in the expression of phosphorylated Smad1 and Smad2/3. Blockade of calcitonin gene-related peptide (CGRP) receptors with CGRP8-37 worsened the I/R-induced renal inflammation and injury. CONCLUSION: Our data indicate that preserving TRPV1 expression and function may prevent renal I/R injury in obesity likely through alleviating inflammatory responses. Copyright
BACKGROUND/AIM: Transient receptor potential vanilloid type 1 (TRPV1) has anti-inflammatory properties. The present study aimed to investigate the role of TRPV1 in renal inflammatory responses and tissue injury following renal ischemia-reperfusion (I/R) in diet-induced obese mice. MATERIALS AND METHODS: TRPV1 knockout and wild type mice were fed a normal or western diet (WD) for 23 weeks and were then subjected to renal I/R injury. RESULTS: TRPV1 knockout mice showed enhanced WD-induced renal macrophage infiltration and collagen deposition. Knocking out TRPV1 exacerbated renal I/R-induced increase of malondialdehyde, interleukin-6, monocyte chemoattractant protein-1, and NF-ĸB in obese mice. Similar results were observed in the expression of phosphorylated Smad1 and Smad2/3. Blockade of calcitonin gene-related peptide (CGRP) receptors with CGRP8-37 worsened the I/R-induced renal inflammation and injury. CONCLUSION: Our data indicate that preserving TRPV1 expression and function may prevent renal I/R injury in obesity likely through alleviating inflammatory responses. Copyright
Authors: Carla F Franco-Penteado; Ivani A De Souza; Enilton A Camargo; Simone A Teixeira; Marcelo N Muscara; Gilberto De Nucci; Edson Antunes Journal: J Pharmacol Exp Ther Date: 2004-12-03 Impact factor: 4.030